Abstract
Once thought to be a degenerative joint condition limited to the degeneration of cartilage, osteoarthritis (OA) is now known to be a complex combination of genetic, metabolic, biomechanical, and biochemical changes involving the entire joint and surrounding tissues. OA generally has a predilection for larger weight-bearing joints such as knees, hips, and the spine. Risk factors include age, female gender, genetics, bone density, and body weight. Most treatment for OA involves pain relief, maximizing joint function, and maintaining quality of life through pharmacologic and nonpharmacologic means. No pharmacologic intervention has conclusively been shown to alter disease progression. Oral and topical medications can alleviate symptoms, with acetaminophen often used as a first-line treatment and an emerging trend toward increased use of topical agents earlier and more often in the course of OA. A comprehensive rehabilitative approach to OA is preferred for disease management, including self-management interventions. Lifestyle changes such as exercise and weight loss have both been shown to be effective. Exercise should consist of joint protection techniques, stretching, strengthening, and aerobic training. Intra-articular corticosteroid injections are often used when oral/topical medications are ineffective. Procedures such as the intra-articular injection of botulinum toxin, platelet-rich plasma, and mesenchymal stem cell injections are becoming more widely used, but further research is needed.
Keywords
joint pain, osteoarthritis, rehabilitation
| Synonym | |
| |
| ICD-10 Codes | |
| M15.9 | Generalized osteoarthritis |
| M19.91 | Primary osteoarthritis, unspecified site |
| M19.93 | Secondary osteoarthritis, unspecified site |
| M19.90 | Unspecified osteoarthritis, unspecified site |
| M12.50 | Traumatic arthropathy, unspecified |
| M12.9 | Arthropathy, unspecified |
Definition
Osteoarthritis (OA) is generally considered to comprise a family of degenerative joint disorders characterized by specific clinical and radiographic findings. OA is the most prevalent chronic joint disease and has become the most common cause of walking disability in older adults in the United States. It is estimated that almost 31 million adults have clinical OA, and the total cost for all arthritis, including OA, is more than 2% of the US gross domestic product. With the aging of the population and the higher incidence of obesity, the disease burden of OA is likely to continue to increase; it is projected that by 2020 it will be the fourth leading cause of disability globally.
OA has traditionally been thought of as the “wear and tear” form of arthritis limited to cartilage degeneration. It is actually a complex combination of genetic, metabolic, biomechanical, and biochemical joint changes that can involve the entire joint and surrounding tissues. The sequence in which joint structures are affected can vary, but the hallmark of OA is the early failure of normal cartilage remodeling causing cartilage degeneration ( Fig. 140.1 ) in response to stress or injury. More recent evidence implicates bone changes and synovial inflammation as also integral to the pathologic process of OA. As a whole, OA is characterized by the degradation and loss of articular cartilage, hypertrophic bone changes with osteophyte formation, subchondral bone remodeling appearing as sclerosis or cysts, chronic synovitis or inflammation of the synovial membrane, and pathology of the joint capsule and surrounding ligaments/tendons.
Joint involvement in OA has a predilection for weight-bearing joints. Common sites of involvement are the hips, knees, hands, feet, and spine. Less common sites of involvement are the ankles, wrists, shoulders, elbows, and sacroiliac joints. Secondary arthritis may become manifest with an atypical pattern of joint involvement.
OA can be classified into two groups: primary and secondary. Primary or idiopathic OA can be localized or generalized. Localized OA usually involves a single joint; generalized OA is the involvement of three or more joints. Secondary OA is due to a specific condition known to cause or to worsen the development of OA ( Table 140.1 ).
|
Multiple risk factors have been linked to the development of OA ( Table 140.2 ). Systemic factors include age, gender, genetics, bone mineral density, and body weight. Age is one of the strongest risk factors for OA. Female gender is associated with higher prevalence of symptomatic knee, hip, and hand OA. Heritable genetic traits of OA are complex and not felt to be due to a defect in a single gene; instead, more recent studies support a polygenic inheritance pattern. Some genetic markers strongly implicated in OA include the GDF5 gene in chromosome 7q22. There is a relationship between bone mineral density and OA. Overweight individuals are shown to be at greater risk for OA, especially in weight-bearing joints like the knee. However, metabolic factors related to obesity have been implicated in the development of OA—a finding based on the association of obesity and OA of a non-weight-bearing joint such as the hand. Other studies have associated OA with metabolic factors such as type 2 diabetes, hypertension, and hyperlipidemia, with one study showing diabetes to be a factor in the progression of narrowing of the knee joint space in men with established OA. Although there has been discussion regarding the role of vitamin deficiencies, there is no consensus regarding the effect of vitamin supplementation in OA. More recent studies have shown vitamin B complex to improve knee pain in OA.
| Systemic Factors |
|
| Biomechanical Factors |
|
Local biomechanical factors implicated in OA include previous joint injury, joint malalignment, anatomic variation or abnormalities in bone, and muscle weakness. Those with previous injury have a 15% greater lifetime risk of symptomatic knee OA. Lower extremity malalignment may be associated with greater radiographic knee OA. Bone abnormalities such as acetabular dysplasia are associated with a greater incidence of hip OA. Muscle weakness, specifically of the knee extensor muscles, predicts knee OA in most cohorts of women. Historical data have correlated certain sporting activities with OA of specific joints, but there is no conclusive evidence, and the studies that have been done have many confounders that make interpretation inconclusive.
Symptoms
Patients usually complain of pain, stiffness, reduced movement, and swelling in the affected joints, which is exacerbated with activity and relieved by rest. Pain at rest or at night suggests severe disease or another diagnosis. Early-morning stiffness, if present, typically lasts for less than 30 minutes. Joint tenderness and crepitus on movement may also be present. Swelling may be due to bone deformity, such as osteophyte formation, or an effusion caused by an accumulation of synovial fluid. Systemic symptoms are absent.
In early disease, pain is usually gradual in onset and mild in intensity. Pain is typically self-limited or intermittent and tends to worsen as the day progresses. Patients with advanced disease may describe a sense of grinding or locking with joint motion and buckling or instability of joints during demanding tasks. Periarticular muscle pain may be prominent. Patients may complain of fatigue if biomechanical changes lead to increased energy requirements for activities of daily living. Overuse of muscle groups can lead to the development of pain syndromes in other parts of the musculoskeletal system.
Physical Examination
Joint Examination
The diagnosis of OA involves assessment of the affected joints for common clinical features ( Table 140.3 ). These usually include tenderness, bone enlargement, and malalignment. Osteophytes, joint-surface irregularity, or chronic disuse may also result in decreased range of motion, pain, effusion, and crepitus. Locking during range of motion may suggest loose bodies, floating cartilage fragments in the joint, or meniscal tears. Joint contracture can result from holding a joint in slight flexion, which is less painful for inflamed or swollen joints. There may be secondary abnormalities in joints above or below the primarily involved joint. Joints must be assessed bilaterally because asymptomatic joints may also have abnormal findings.
|
|
|
|
|
|
|
Neuromuscular and General Examination
A thorough musculoskeletal examination should include inspection, palpation of soft tissues surrounding the joint of interest, and assessment of both muscle strength and flexibility. First, gait should be observed. There may be an antalgic gait or a slow gait pattern because of pain in a specific joint. If the patient uses a cane, appropriate use of the cane should be assessed during gait.
Both functional strength and manual muscle testing should be performed. Periarticular muscle atrophy and weakness may be present in chronic OA, but functional tests like sit-to-stand testing, which often provokes pain in OA of the knee and hip, may be more informative. Palpation and dynamic testing of soft tissues may differentiate pain from tendinopathy or bursitis from OA. Joint-specific provocative maneuvers may help to isolate the source in symptomatic patients with poorly localized pain. A careful neurologic examination should be performed to make sure that pain is not due to nerve impingement or a neuropathic process.
Clinicians may also consider performing a general examination. Evaluation of other systems may also help to differentiate primary OA from secondary OA due to a systemic process. Because obesity is the most important modifiable risk factor for OA, assessment of the patient’s body mass index is essential.
Functional Limitations
Functional limitations will depend on the joints affected by OA. Patients with disease in the hips and knees will have impairments in mobility, locomotion, and activities of daily living involving the lower body. For example, loss of hip external rotation commonly seen in OA can impair one’s ability to sit cross-legged and therefore impact lower extremity dressing. Patients may complain of increasing difficulty with ascending and descending stairs, walking, making chair or toileting transfers, and lower body dressing and grooming. Degeneration in the shoulders or hands limits vocational and recreational activities, self-care, and upper body activities of daily living. Patients may initially have trouble with using the computer or lifting boxes, which then progresses to difficulties with activities of daily living like feeding, grooming, bathing, and dressing. OA of the spine can result in limitations with all mobility.
Diagnostic Studies
Although imaging studies are not needed to confirm the diagnosis, plain radiographs may help to elucidate the severity of joint damage and progression of OA. The classic findings include asymmetric joint space narrowing without periarticular joint erosions, osteophytes at joint margins, subchondral sclerosis, and subchondral cyst formation. There is a well-demonstrated discordance between x-ray findings and symptoms in OA. Asymptomatic individuals, particularly the elderly, may have significant radiographic disease, whereas severe pain and dysfunction can occur in the setting of limited radiologic changes. Computed tomography scans, ultrasonography, and magnetic resonance imaging (MRI) are typically not needed for the evaluation of OA but can be helpful in providing better visualization not only for the evaluation of OA severity but also for the identification of other pathologic tissue processes and diagnosis. MRI in particular can identify early OA changes such as cartilage defects before they are seen on routine x-rays.
Routine laboratory test results should be normal, and laboratory testing is usually not needed in uncomplicated cases of OA. If laboratory tests are available, clinicians should take care in interpreting the results. There is a high prevalence of laboratory abnormalities in elderly people, such as a raised erythrocyte sedimentation rate or anemia because of comorbid conditions. Autoimmune markers may be useful to differentiate OA from other musculoskeletal disorders such as inflammatory arthritides.
Joint aspiration should be pursued in patients with significant joint effusion or inflammation. Analysis of joint fluid can be helpful in ruling out a crystal deposition disease such as gout or pseudogout, inflammatory arthritis, or infectious arthritis. In contrast to other arthritides, synovial fluid in OA is usually clear, with normal viscosity and leukocyte counts typically less than 1500 to 2000/mm 3 .
Related posts:
Stay updated, free articles. Join our Telegram channel
Full access? Get Clinical Tree
